Previous work from our laboratory and others has demonstrated that prenatal ethanol exposure can result in demasculinization and feminization of sexually dimorphic behaviors in males. This effect results in large part from the inhibitory influence of ethanol on fetal and neonatal testosterone production. The prenatal surge of testosterone is absent and the postnatal surge is attenuated in fetal alcohol exposed (FAE) males. The normal occurrence and timing of these surges is critical to the sexual differentiation of the male brain. Gonadal steroids also have an organizational influence on developing vasopressin and oxytocin systems, both of which are involved in the expression of a range of adult behaviors, including sexual behavior, water consumption and regulation of circadian rhythms in locomotor activity patterns. Preliminary data demonstrate behavioral alterations in FAE animals indicating that these systems may be altered by in utero ethanol. In addition, we have observed significant decreases in vasopressin levels in brain. We have proposed to study the influence of ethanol on the development of these systems in FAE males using in situ hybridization for oxytocin and vasopressin mRNA. Behavioral studies are designed to characterize the influence of prenatal ethanol exposure on circadian rhythms in adulthood. Studies are also designed to study the responsiveness of the suprachiasmatic nucleus in the sesw animals. Other studies will examine the therapeutic efficacy of testosterone replacement during the critical prenatal period to ameliorate some of the effects of ethanol on sexual differentiation in males. Data derived from these studies will be important in the development of endocrine strategies to treat children exposed to alcohol in utero. They will also add significantly to our understanding of the neuroendocrine contribution to the control of circadian rhythms.